The secretion of parathyroid hormone (PTH) and calcitonin (CT) appears to be regulated primarily by the calcium ion (Ca ions) concentration bathing the respective glands. The importance of autonomic modulation is established for other hormones (insulin, glucagon), but data supporting such neural control of PTH and CT secretion are less definitive. Beta-adrenergic agonists stimulate secretion of both PTH and CT, and alpha-adrenergic agonists inhibit CT release; such effects are independent of ambient Ca ions. It is uncertain whether these pharmacologic findings illuminate normal physiology, but if they do, analogy with other endocrine glands suggests that adrenergic autonomic mechanisms may be functionally important to calcium homeostasis. A component of the autonomic nervous system might be the long-sought, non-Ca ions tropic influence on the parathyroid glands. The goals of the proposed studies are to establish, in the dog and rat, whether the autonomic nervous system is capable of affecting PTH and CT secretion by adrenergic or cholinergic mechanisms; and to establish the importance of both arms of the autonomic nervous system (sympathetic and parasympathetic) in physiologic regulation of PTH and CT. Sensitive micro-radioimmunoassays for canine and murine PTH and CT will be used to assess affects of sympathetic/parasympathetic electrostimulation, adrenergic/cholinergic blockage, chemical sympathectomy (6-OHDA), vagotomy, and organ transplantation (denervation) upon physiologic responses of the parathyroid and parafollicular cells to a variety of stimuli. These animal models will permit experiments which cannot be done in man, but which could contribute to understanding such human disease states as primary parathyroid hyperplasia or C-cell hyperplasia.